Molecular Biotechnology最新文献

Transcription Factor STAT3-Activated LDHB Promotes Tumor Properties of Endometrial Cancer Cells by Inducing MDH2 Expression. 转录因子 STAT3 激活的 LDHB 通过诱导 MDH2 表达促进子宫内膜癌细胞的肿瘤特性

IF 2.4 4区生物学

Molecular Biotechnology Pub Date : 2025-02-01 Epub Date: 2024-02-21 DOI: 10.1007/s12033-024-01067-z

Li Shen, Juan Wang, Yanxia Li, Cuizhen Sun, Minjie Teng, Xiaohe Ye, Xiaomin Feng

{"title":"Transcription Factor STAT3-Activated LDHB Promotes Tumor Properties of Endometrial Cancer Cells by Inducing MDH2 Expression.","authors":"Li Shen, Juan Wang, Yanxia Li, Cuizhen Sun, Minjie Teng, Xiaohe Ye, Xiaomin Feng","doi":"10.1007/s12033-024-01067-z","DOIUrl":"10.1007/s12033-024-01067-z","url":null,"abstract":"The pathogenesis of endometrial cancer (EC) involves the regulation of lactate dehydrogenases. However, the role and mechanism of lactate dehydrogenase-B (LDHB) in EC progression have not been studied. The mRNA levels of LDHB and malate dehydrogenase 2 (MDH2) were detected by quantitative real-time polymerase chain reaction. Protein expression was checked by western blotting and immunohistochemistry assays. Cell proliferation, apoptosis, and invasion were analyzed by 5-Ethynyl-2'-deoxyuridine, transwell, and flow cytometry assay, respectively. Glycolysis was investigated using Glucose Assay Kit, CheKine™ Micro Lactate Assay Kit, and ADP/ATP ratio assay kit. An in vivo tumor formation assay was conducted to disclose the effect of LDHB on tumor growth in vivo. The associations among signal transducer and activator of transcription 3 (STAT3), LDHB, and MDH2 were predicted through JASPAR or GeneMANIA online database and identified by chromatin immunoprecipitation assay, dual-luciferase reporter assay, and co-immunoprecipitation assay. LDHB expression was increased in EC tissues and cells in comparison with normal endometrial tissues and human endometrial stromal cells. LDHB had the potential as a biomarker to predict the prognosis of EC patients. In addition, LDHB knockdown inhibited the proliferation, invasion, and glycolysis and promoted apoptosis of RL95-2 and Ishikawa cells. LDHB knockdown inhibited tumor property of Ishikawa cells in vivo. STAT3 bound to the promoter region of LDHB, and STAT3 silencing-induced effects were relieved after LDHB upregulation. LDHB interacted with and regulated MDH2 expression. Moreover, MDH2 overexpression rescued LDHB knockdown-induced effects on EC cell phenotypes. STAT3-activated LDHB promoted endometrial cancer cell malignancy by inducing MDH2 production.","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":" ","pages":"562-574"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139913022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Circ_0082374 Promotes the Tumorigenesis and Suppresses Ferroptosis in Non-small Cell Lung Cancer by Up-Regulating GPX4 Through Sequestering miR-491-5p. Circ_0082374 通过螯合 miR-491-5p 上调 GPX4 促进非小细胞肺癌的肿瘤发生并抑制其铁蛋白沉积。

IF 2.4 4区生物学

Molecular Biotechnology Pub Date : 2025-02-01 Epub Date: 2024-03-04 DOI: 10.1007/s12033-024-01059-z

Zongyu Li, Mengdi Fan, Zhibo Zhou, Xianyin Sang

{"title":"Circ_0082374 Promotes the Tumorigenesis and Suppresses Ferroptosis in Non-small Cell Lung Cancer by Up-Regulating GPX4 Through Sequestering miR-491-5p.","authors":"Zongyu Li, Mengdi Fan, Zhibo Zhou, Xianyin Sang","doi":"10.1007/s12033-024-01059-z","DOIUrl":"10.1007/s12033-024-01059-z","url":null,"abstract":"Circular RNAs (circRNAs) have been identified to be dysregulated in non-small cell lung cancer (NSCLC) and implicated in the progression of this cancer. Here, this work aimed to investigate the role and mechanism of circ_0082374 on NSCLC progression. Levels of circ_0082374, miR-491-5p, GPX4 (glutathione peroxidase 4) and epithelial-mesenchymal transition (EMT)-related proteins were examined by quantitative real-time PCR or western blotting, respectively. Cell proliferation and metastasis were detected using cell counting kit-8, colony formation, EdU, transwell, and Scratch assays. Cell ferroptosis was evaluated by measuring cell survival after the treatment of different ferroptosis inducers or inhibitors, as well as the accumulation of intracellular reactive oxygen species (ROS), ferrous iron (Fe2+) and malondialdehyde (MDA). The binding between miR-491-5p and circ_0082374 or GPX4 was confirmed using dual-luciferase reporter and RNA pull-down assays. In vivo experiments were conducted using murine xenograft assay and immunohistochemistry. Circ_0082374 was a stable circRNA with high expression in NSCLC tissues and cells. Functionally, circ_0082374 silencing suppressed NSCLC cell proliferation and metastasis. Moreover, its down-regulation enhanced ferroptosis by decreasing iron and lipid peroxidation accumulation. Mechanistically, circ_0082374 could indirectly up-regulate GPX4 expression via miR-491-5p, indicating the circ_0082374/miR-491-5p/GPX4 competitive endogenous RNAs (ceRNA) network. Rescue experiments demonstrated that the miR-491-5p/GPX4 axis mediated the regulatory effects of circ_0082374 exerted on NSCLC cells. Moreover, knockdown of circ_0082374 impeded NSCLC growth and EMT via regulating miR-491-5p and GPX4. Circ_0082374 silencing could suppress NSCLC cell proliferation, metastasis and induce ferroptosis through miR-491-5p/GPX4 axis, suggesting a novel therapeutic approach for NSCLC patients.","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":" ","pages":"484-495"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140028522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular Mutations in Histiocytosis: A Comprehensive Survey of Genetic Alterations. 组织细胞增生症的分子突变：组织细胞增生症的分子突变：遗传变异的全面调查。

IF 2.4 4区生物学

Molecular Biotechnology Pub Date : 2025-02-01 Epub Date: 2024-02-20 DOI: 10.1007/s12033-024-01072-2

Padmini Pai, Arnav Nirmal, Lian Mathias, Siya Jain, Manasa Gangadhar Shetty, Babitha Kampa Sundara

{"title":"Molecular Mutations in Histiocytosis: A Comprehensive Survey of Genetic Alterations.","authors":"Padmini Pai, Arnav Nirmal, Lian Mathias, Siya Jain, Manasa Gangadhar Shetty, Babitha Kampa Sundara","doi":"10.1007/s12033-024-01072-2","DOIUrl":"10.1007/s12033-024-01072-2","url":null,"abstract":"Histiocytosis represents a group of uncommon disorders characterized by the abnormal accumulation of specialized immune cells, such as macrophages, dendritic cells, or monocyte-derived cells, in various tissues and organs. Over 100 distinct subtypes have been documented, each displaying a broad spectrum of clinical presentations and histological characteristics. Till today, histiocytosis has been addressed through a combination of chemotherapy, radiotherapy, and surgery, with varying responses from individual patients. Due to its atypical symptoms, it has been prone to misdiagnosis. Advances in our understanding of the cellular and molecular aspects of these conditions are paving the way for improved diagnostic methods and targeted therapies. Researchers have extensively investigated various mutations in patient samples. However, no paper has yet provided a comprehensive summary of the collective analysis of mutations and pathways. Hence, this paper consolidates research efforts that specifically concentrate on gene mutations identified in patient samples of different subtypes of histiocytosis. These insights are essential for developing targeted therapies and improving diagnosis. Further, it provides potential insights to enhance the development of more effective therapeutic approaches for rare diseases.","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":" ","pages":"438-455"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11711569/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139906083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Circ_0007351 Exerts an Oncogenic Role In Colorectal Cancer Depending on the Modulation of the miR-5195-3p/GPRC5A Cascade. Circ_0007351 依靠调控 miR-5195-3p/GPRC5A 级联在结直肠癌中发挥致癌作用

IF 2.4 4区生物学

Molecular Biotechnology Pub Date : 2025-02-01 Epub Date: 2024-02-22 DOI: 10.1007/s12033-024-01071-3

Aijun He, Fangxin Liao, Xiaohui Lin

{"title":"Circ_0007351 Exerts an Oncogenic Role In Colorectal Cancer Depending on the Modulation of the miR-5195-3p/GPRC5A Cascade.","authors":"Aijun He, Fangxin Liao, Xiaohui Lin","doi":"10.1007/s12033-024-01071-3","DOIUrl":"10.1007/s12033-024-01071-3","url":null,"abstract":"Circular RNAs (circRNAs) exert critical functions in colorectal cancer development. In this work, we wanted to elucidate the functional role and regulatory mechanism of circ_0007351 in colorectal cancer. For quantification of circ_0007351, microRNA (miR)-5195-3p and G Protein-coupled receptor class C group 5 member A (GPRC5A), a qRT-PCR, immunoblotting or immunohistochemistry assay was performed. Effects of circ_0007351/miR-5195-3p/GPRC5A cascade were evaluated by determining cell viability, proliferation, colony formation, motility, and invasion. Relationships among variables were assessed by dual-luciferase reporter assay. Animal studies were performed to evaluate circ_0007351's function in the growth of xenograft tumors. Circ_0007351 was markedly up-regulated in colorectal cancer tissues and cells. Down-regulation of circ_0007351 hindered cell growth, migration and invasiveness. Also, circ_0007351 depletion exerted a suppressive function in colorectal cell xenograft growth in vivo. Mechanistically, circ_0007351 sponged miR-5195-3p to sequester miR-5195-3p. Reduction of available miR-5195-3p neutralized the effects of circ_0007351 down-regulation on cell phenotypes. MiR-5195-3p directly targeted and inhibited GPRC5A. Circ_0007351 regulated GPRC5A expression by sponging miR-5195-3p. Moreover, the effects of circ_0007351 down-regulation on cell functional phenotypes were due to in part the reduction of GPRC5A expression. Our findings show that circ_0007351 down-regulation impedes proliferation, motility, and invasiveness in colorectal cancer cells at least in part via the regulation of the miR-5195-3p/GPRC5A cascade, highlighting that circ_0007351 inhibition may have a potential therapeutic value for colorectal cancer.","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":" ","pages":"617-627"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139932062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Platelet-Derived Microvesicles Mediate Cardiomyocyte Ferroptosis by Transferring ACSL1 During Acute Myocardial Infarction. 急性心肌梗死期间血小板衍生的微囊泡通过转移 ACSL1 介导心肌细胞铁凋亡

IF 2.4 4区生物学

Molecular Biotechnology Pub Date : 2025-02-01 Epub Date: 2024-03-11 DOI: 10.1007/s12033-024-01094-w

Yunfeng Zhao, Rui Cui, Ran Du, Chunmei Song, Fei Xie, Lin Ren, Junquan Li

{"title":"Platelet-Derived Microvesicles Mediate Cardiomyocyte Ferroptosis by Transferring ACSL1 During Acute Myocardial Infarction.","authors":"Yunfeng Zhao, Rui Cui, Ran Du, Chunmei Song, Fei Xie, Lin Ren, Junquan Li","doi":"10.1007/s12033-024-01094-w","DOIUrl":"10.1007/s12033-024-01094-w","url":null,"abstract":"Acute myocardial infarction (AMI) is one of the critical health conditions often caused by the rupture of unstable coronary artery plaque, triggering a series of events, such as platelet activation, thrombus formation, coronary artery blockage, lasted severe ischemia, and hypoxia in cardiomyocytes, and culminating in cell death. Platelet-derived microvesicles (PMVs) act as intermediates for cellular communication. Nevertheless, the role of PMVs in myocardial infarction remains unclear. Initially, AMI-related messenger ribose nucleic acid (mRNA) and micro RNA (miRNA) datasets from the Gene Expression Omnibus (GEO) database were analyzed, specifically focusing on the expressed genes associated with Ferroptosis. Further, a miRNA-mRNA regulatory network specific to AMI was constructed. Then, the effect of PMVs on cardiomyocyte survival was further confirmed through in vitro experiments. High ACSL1 expression was observed in the platelets of AMI patients. The gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed that ACSL1, located in the mitochondria, played a key role in the PPAR signaling pathway. The elevated ACSL1 expression in a co-culture model of PMVs and AC16 cardiomyocytes significantly increased the AC16 cell Ferroptosis. Further, we validated that the platelet ACSL1 expression could be regulated by hsa-miR-449a. Together, these findings suggested that platelet ACSL1 could trigger myocardial cell death via PMV transport. In addition, this research provided a theoretical framework for attenuating myocardial cell Ferroptosis in patients with acute myocardial infarction.","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":" ","pages":"790-804"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140102045","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Future of Gene Therapy: A Review of In Vivo and Ex Vivo Delivery Methods for Genome Editing-Based Therapies. 基因疗法的未来：基于基因组编辑疗法的体内和体外给药方法综述》。

IF 2.4 4区生物学

Molecular Biotechnology Pub Date : 2025-02-01 Epub Date: 2024-02-16 DOI: 10.1007/s12033-024-01070-4

Olga Volodina, Svetlana Smirnikhina

{"title":"The Future of Gene Therapy: A Review of In Vivo and Ex Vivo Delivery Methods for Genome Editing-Based Therapies.","authors":"Olga Volodina, Svetlana Smirnikhina","doi":"10.1007/s12033-024-01070-4","DOIUrl":"10.1007/s12033-024-01070-4","url":null,"abstract":"The development of gene therapy based on genome editing has opened up new possibilities for the treatment of human genetic disorders. This field has developed rapidly over the past few decades, some genome editing-based therapies are already in phase 3 clinical trials. However, there are several challenges to be addressed before widespread adoption of gene editing therapy becomes possible. The main obstacles in the development of such therapy are safety and efficiency, so one of the biggest issues is the delivery of genetic constructs to patient cells. Approaches in genetic cargo delivery divide into ex vivo and in vivo, which are suitable for different cases. The ex vivo approach is mainly used to edit blood cells, improve cancer therapy, and treat infectious diseases. To edit cells in organs researches choose in vivo approach. For each approach, there is a fairly large set of methods, but, unfortunately, these methods are not universal in their effectiveness and safety. The focus of this article is to discuss the current status of in vivo and ex vivo delivery methods used in genome editing-based therapy. We will discuss the main methods employed in these approaches and their applications in current gene editing treatments under development.","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":" ","pages":"425-437"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139741455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An Analysis Regarding the Association Between DAZ Interacting Zinc Finger Protein 1 (DZIP1) and Colorectal Cancer (CRC). DAZ互作锌指蛋白1（DZIP1）与结直肠癌（CRC）之间的关系分析

IF 2.4 4区生物学

Molecular Biotechnology Pub Date : 2025-02-01 Epub Date: 2024-02-09 DOI: 10.1007/s12033-024-01065-1

Yu Zhang, Yuan-Jie Liu, Jia Mei, Zhao-Xu Yang, Xiao-Ping Qian, Wei Huang

{"title":"An Analysis Regarding the Association Between DAZ Interacting Zinc Finger Protein 1 (DZIP1) and Colorectal Cancer (CRC).","authors":"Yu Zhang, Yuan-Jie Liu, Jia Mei, Zhao-Xu Yang, Xiao-Ping Qian, Wei Huang","doi":"10.1007/s12033-024-01065-1","DOIUrl":"10.1007/s12033-024-01065-1","url":null,"abstract":"Colorectal cancer (CRC) is the third most common malignant disease worldwide, and its incidence is increasing, but the molecular mechanisms of this disease are highly heterogeneous and still far from being fully understood. Increasing evidence suggests that fibrosis mediated by abnormal activation of fibroblasts based in the microenvironment is associated with a poor prognosis. However, the function and pathogenic mechanisms of fibroblasts in CRC remain unclear. Here, combining scrna-seq and clinical specimen data, DAZ Interacting Protein 1 (DZIP1) was found to be expressed on fibroblasts and cancer cells and positively correlated with stromal deposition. Importantly, pseudotime-series analysis showed that DZIP1 levels were up-regulated in malignant transformation of fibroblasts and experimentally confirmed that DZIP1 modulates activation of fibroblasts and promotes epithelial-mesenchymal transition (EMT) in tumor cells. Further studies showed that DZIP1 expressed by tumor cells also has a driving effect on EMT and contributes to the recruitment of more fibroblasts. A similar phenomenon was observed in xenografted nude mice. And it was confirmed in xenograft mice that downregulation of DZIP1 expression significantly delayed tumor formation and reduced tumor size in CRC cells. Taken together, our findings suggested that DZIP1 was a regulator of the CRC mesenchymal phenotype. The revelation of targeting DZIP1 provides a new avenue for CRC therapy.","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":" ","pages":"527-547"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139707237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Long Noncoding RNA GAS5-Involved Progression of Neonatal Hydrocephalus and Inflammatory Responses. 长非编码 RNA GAS5 与新生儿脑积水的进展和炎症反应有关

IF 2.4 4区生物学

Molecular Biotechnology Pub Date : 2025-02-01 Epub Date: 2024-03-01 DOI: 10.1007/s12033-024-01077-x

Bin Zou, Qin Zhang, Hui Gan, Yue Qin, Yudong Zhou, Xuan Zhai, Ping Liang

{"title":"Long Noncoding RNA GAS5-Involved Progression of Neonatal Hydrocephalus and Inflammatory Responses.","authors":"Bin Zou, Qin Zhang, Hui Gan, Yue Qin, Yudong Zhou, Xuan Zhai, Ping Liang","doi":"10.1007/s12033-024-01077-x","DOIUrl":"10.1007/s12033-024-01077-x","url":null,"abstract":"Intraventricular hemorrhage results in posthemorrhagic hydrocephalus (PHH). Neonatal hydrocephalus remains a challenging disease due to the high failure rate of all management strategies. We evaluated long noncoding RNA growth arrest-specific 5 (GAS5)-mediated network in neonatal hydrocephalus, providing a new direction for the treatment of hydrocephalus. The PHH model was constructed in neonatal rats after intracerebroventricular injection with GAS5, miR-325-3p, and chaperonin containing T-complex protein 1, subunit 8 (CCT8) plasmids, or oligonucleotides. Next, behavioral tests, measurement of serum inflammation, observation of brain tissue pathology, and calculation of hemoglobin and brain water contents were implemented. GAS5, miR-325-3p, and CCT8 expression, in combination with their interactions, was checked. As the results reported, collagenase infusion induced hydrocephalus, impairing neurological function, enhancing inflammation and neuronal apoptosis, and increasing hemoglobin and brain water contents. GAS5 and CCT8 were up-regulated, while miR-325-3p was down-regulated in hydrocephalic rats. Downregulating GAS5/CCT8 or upregulating miR-325-3p could inhibit inflammatory response and improve neurological function in young hydrocephalic rats. GAS5 promotes CCT8 expression through sponge adsorption of miR-325-3p. GAS5 silencing-mediated protections against hydrocephalus were counteracted by CCT8 overexpression. In summary, GAS5 aggravates neonatal hydrocephalus and inflammatory responses in a way of leasing miR-325-3p-involved regulation of CCT8.","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":" ","pages":"661-672"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140013012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

YY1 Contributes to the Inflammatory Responses of Mycobacterium tuberculosis-Infected Macrophages Through Transcription Activation-Mediated Upregulation TLR4. YY1 通过转录激活 TLR4 上调，促进结核分枝杆菌感染的巨噬细胞的炎症反应。

IF 2.4 4区生物学

Molecular Biotechnology Pub Date : 2025-02-01 Epub Date: 2024-03-16 DOI: 10.1007/s12033-024-01093-x

Xing Yang, Yu Chen, Bingshuang Pu, Xuan Yuan, Jiaojiao Wang, Chun Chen

{"title":"YY1 Contributes to the Inflammatory Responses of Mycobacterium tuberculosis-Infected Macrophages Through Transcription Activation-Mediated Upregulation TLR4.","authors":"Xing Yang, Yu Chen, Bingshuang Pu, Xuan Yuan, Jiaojiao Wang, Chun Chen","doi":"10.1007/s12033-024-01093-x","DOIUrl":"10.1007/s12033-024-01093-x","url":null,"abstract":"Tuberculosis (TB) is a chronic respiratory infectious disease and is induced by Mycobacterium tuberculosis (M.tb) infection. Macrophages serve as the cellular home in immunoreaction against M.tb infection, which is tightly regulated through Toll-like receptor 4 (TLR4) expression. Therefore, this study is designed to explore the role and mechanism of TLR4 in mycobacterial injury in human macrophages (THP-1 cells) after M.tb infection. Cell proliferation and apoptosis were assessed using MTT, EdU, and flow cytometry assays. ELISA kits were utilized to assess the levels of Interleukin-6 (IL-6), IL-1β, and tumor necrosis factor α (TNF-α). The binding between Yin-Yang-1 (YY1) and TLR4 promoter was predicted by JASPAR and verified using Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. M.tb infection might repress THP-1 cell proliferation, and induce cell apoptosis and inflammatory response in a multiplicity of infection (MOI)-dependent manner. Moreover, M.tb infection increased the expression of TLR4 in HTP-1 cells in an MOI-dependent way, and its downregulation might overturn M.tb infection-mediated HTP-1 cell damage and inflammatory response. At the molecular level, YY1 was a transcription factor of TLR4 and promoted TLR4 transcription via binding to its promoter region. Besides, YY1 might activate the NF-kB signaling pathway via regulating TLR4. Meanwhile, TLR4 inhibitor BAY11-7082 might overturn the repression effect of TLR4 on M.tb-infected HTP-1 cell damage. YY1-activated TLR4 might aggravate mycobacterial injury in human macrophages after M.tb infection by the NF-kB pathway, providing a promising therapeutic target for TB treatment.","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":" ","pages":"778-789"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140140480","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lectin: A Molecular Tool in Cancer Diagnosis and Therapy with Special Reference to Reproductive Cancers. Lectin：癌症诊断和治疗的分子工具，特别是生殖系统癌症。

IF 2.4 4区生物学

Molecular Biotechnology Pub Date : 2025-02-01 Epub Date: 2024-03-08 DOI: 10.1007/s12033-024-01086-w

Rachna M Pallar, Shubhangi K Pingle, Avinash Shivaji Gaikwad, Naveen S Yennam, N Raju, Panja Kumar, Vinay Kumar Adepu, Rajani G Tumane, Chennuru Veeranjaneyulu, Kartikey Matte

{"title":"Lectin: A Molecular Tool in Cancer Diagnosis and Therapy with Special Reference to Reproductive Cancers.","authors":"Rachna M Pallar, Shubhangi K Pingle, Avinash Shivaji Gaikwad, Naveen S Yennam, N Raju, Panja Kumar, Vinay Kumar Adepu, Rajani G Tumane, Chennuru Veeranjaneyulu, Kartikey Matte","doi":"10.1007/s12033-024-01086-w","DOIUrl":"10.1007/s12033-024-01086-w","url":null,"abstract":"The prevalence of cancer deaths globally and domestically is higher especially due to the deferment of diagnosis and lack of facilities for women's reproductive cancers. The present review focussed to explore the application of lectins in cancer theranostics. Though there is cancer diagnostic and treatment available there is no promising early diagnostic tool and effective treatment available for the cancer which is the major concern. Lectins are cellulose-binding proteins that are strongly determined in saccharide groups of glycans, glycopeptides, or glycolipids. In the concomitance of events in cells, carbohydrates, and proteins, lectins play an important role. Lectins bind superiorly to the cancer cell membrane and their receptors induce the cytotoxic effect, which results in caspase-mediated cell death, and prohibits tumour development. Lectin snuffing also reveals polyamine stocks and impedes the growth of cancerous cells. They affect the cell cycle by non-apoptotic aggregation, seizure of the cell cycle phase G2, M, and the mediation of caspases. It can also adversely affect the action of telomerase and hinder vascularisation. They promote immunomodulation and adversely limit protein synthesis. Their easy availability and its characteristics support its use in cancer diagnosis and therapy, despite their small corollary effects. Future investigations recommend focussing more on the key applications of lectin by reducing its concurrent effects and carrying out more in-vitro investigations. However, the use of lectin formulations for cancer theranostics is a new area in cancer detection and treatment. In this review, plant lectin appears to be a potential target for cancer research in the fields of diagnosis and theranostics.","PeriodicalId":18865,"journal":{"name":"Molecular Biotechnology","volume":" ","pages":"456-468"},"PeriodicalIF":2.4,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140059950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0